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Membrane‐associated phospholipase A1 beta (LIPI) Is an Ewing tumour‐associated cancer/testis antigen
Author(s) -
Foell Juergen L.,
Hesse Manuela,
Volkmer Ines,
Schmiedel Benjamin J.,
Neumann Ingo,
Staege Martin S.
Publication year - 2008
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.21602
Subject(s) - antigen , pathology , immunohistochemistry , cancer , biology , medicine , immunology , genetics
Background Cancer/testis antigens (CTA) represent a heterogeneous group of antigens expressed nearly exclusively in tumour cells and testis. Recently, we identified phospholipase A1 beta (a CTA also known as lipase member I, LIPI) as a gene with high expression in Ewing family tumours (EFT). In the present paper we analyzed expression of LIPI in a panel of normal tissues and tumour samples. Procedure The expression of CTA in EFT and normal tissues was analyzed by using DNA microarray datasets. Expression of LIPI in EFT, a panel of other tumour samples, and normal tissues was analyzed by using RT‐PCR and quantitative RT‐PCR. Results LIPI was expressed in EFT samples but not in other investigated tumour samples. Expression of LIPI in normal tissues was restricted to testis and thyroid. However, expression in these tissues was low compared with EFT. Interestingly testis as well as thyroid expressed all analyzed EFT‐associated transcripts, suggesting that these tissues harbour a small cell population with molecular features of EFT. The sensitivity of the LIPI RT‐PCR was similar to the sensitivity of the conventional EWSR1‐FLI1 RT‐PCR, suggesting that LIPI might be useful as additional diagnostic target structure. Conclusions The human cancer/testis antigen LIPI is highly expressed in Ewing family tumours and can be easily detected by RT‐PCR or quantitative RT‐PCR. LIPI might be an interesting target for the development of future diagnostic tools or treatment strategies. Pediatr Blood Cancer 2008;51:228–234. © 2008 Wiley‐Liss, Inc.